A chronic fatigue syndrome (CFS) sufferer reads a passionate letter to a Congressional committee . In the
letter, she describes a multitude of tribulations with which many of us can
readily empathize. She outlines the sloppy, inadequate approach the government
has taken in addressing the illness. She talks about substandard treatment by
the medical community, insurance companies, and Medicaid. And finally, she
eloquently states how disabling her illness is, and how the public is apathetic
and uninformed. Then, in a passionately delivered finale, she shares what she
feels is a solution that will put an end to these problems: these problems will
be solved if we rename the illness myalgic encephalomyelitis.

Mention the term “M.E. advocacy” to someone who is unfamiliar with
traditional M.E. or CFS advocacy approaches, and you may get a blank stare. However, most who are aware of recent advocacy efforts for this disease would be
familiar with ME advocacy. A long-standing advocacy
strategy has developed around two terms, myalgic, denoting muscle pain or
dysfunction, and the brain-central terms encephalomyelitis or encephalopathy.

These efforts have provided a hopeful strategy for many. Many advocates
believe the term myalgic encephalomyelitis will
eventually place the illness on a physiological foundation. Some advocates have
made these two terms the centerpiece of their strategy for eradicating this
devastating disease. One advocate declares, “Let it be made clear that the
campaign to restore the name and recognition of myalgic encephalomyelitis is
well underway. We are prepared to be persistent.”

Is it effective?

But has M.E. advocacy been effective? Is this approach making headway, creating
credibility among the medical community, and reinforcing recent strides in
research? Should we ensure that each of our methods of advocacy conform to M.E
advocacy? Or, does M.E advocacy have limitations, or even cause unwitting damage?

Why the Popularity of M.E.-only advocacy?

There is more than one reason many feel that the term of M.E should be the
foundation of their advocacy efforts. First, M.E. definitions are much closer to
a homogeneous illness that many with CFS describe. The hallmark post-exertional
symptoms of the illness, as well as orthostatic and circulatory dysfunction, are
headlined in the M.E. definition.

Many feel M.E. advocacy takes into account a longstanding heritage, history,
and tradition. Some insist little has changed in our knowledge of the pathology
of the disease in the 50 years since the name , myalgic encephalomyelitis, was created.

Quite a few M.E advocates prefer a term that will emphasize either
brain-predominant fields of research or the symptom of muscle pain. Others feel
that the symptoms and pathology of myalgic encephalopathy would more closely
describe the pain of fibromyalgia syndrome, an illness whose broad symptom set
is not fully recognized. One advocate says: “I would also like to change the
name of FMS (Fibromyalgia) to M.E as it doesn't fully describe the severity of its impact on
sufferers.” She adds that the myalgic in M.E. will help recognize the muscle
pain of “Fibromyalgia, another indescribably debilitating disease that often
goes hand in hand with ME/CFS. ”

Finally, the most likely reason many have placed their advocacy efforts
behind the term has to do with the devastating resonance and serious intonation
of the name itself. As one patient says, “I have found that people take me more
seriously if I say I suffer from myalgic
encpaphalomyelitis, rather than chronic fatigue syndrome, when they
immediately think I am just tired.”

Given these justifications, why would M. E. advocacy not help us achieve
steady, long-term progress? For many years, this style of advocacy has offered
many inspiring hope, simplicity, and a sense of promise. Could so
many be so wrong?

Yes. They could. M.E. advocacy is simple,
and it has been around a long time. But, it doesn't take into
account some very harmful problems.

Making the Brain Foremost…

Beyond the Brain --- Without a doubt, the prefix
encephalo is a term that steers clinicians and researchers to brain predominant
fields of study. One advocate says that, “some patients' symptoms may be
brain-predominant, others muscle myopathy predominant…”

The battle to secure the term M.E. must focus on symptoms of brain
dysfunction. If
we truly desire a brain foremost term to represent the illness, then we must
make a case that a poorly functioning brain is a primary pathological feature of
the illness. This is a political and scientific reality.

And yet, while there is consensus among M.E advocates that the brain should
be the predominantly featured term, there is a longstanding disagreement over
what the appended suffix should be.

Does it really matter if it is ‘opathy’ or ‘itis’

One advocate states that the scientific community has “become entrenched in
their opposition to the adoption of Myalgic Encephalomyelitis.” He goes on to
say that by refusing to name the disease after brain inflammation, the CDC has
conspired by “ choosing to ignore the 50-year clinical history of the disease
the rest of the world called Myalgic Encephalomyelitis.” Later, he urges
patients to continue expending their time and effort on securing the term
encephalomyelitis, claiming the term will eventually help to build public
credibility.

But science is clear that the term encephalitis or
encephalomyelitis (acute
brain or spinal inflammation) has not been shown to be pathologically correct.
As another M.E. advocate correctly explains, this approach is significantly
affecting our credibility. ”We have now reached the point where there just isn't
enough robust scientific evidence to continue to maintain that encephalomyelitis
is a pathologically correct explanation for the type of brain abnormalities that
undoubtedly do occur in this disease.”

As a solution to this problem, M.E. advocates have decided to continue the M.E.
advocacy under 'encephalopathy', a broader
term which describes a
dysfunctional brain state. As one M.E. advocate explains: “…It is possible to argue with the medical establishment that the
term encephalopathy could be applied to these abnormalities, and in so doing the
term M.E. can be maintained with justification.” He continues by saying “it
should be perfectly acceptable for patients to use the term M.E. - even if their
doctors want to refer to CFS…and this is an important step forward.”

However, many assert that encephalopathy would undoubtedly steer public
perception of the illness toward any or every brain-predominant field:
neurology, psychiatry, and psychology -- a grave mistake. Not one of these
fields have been a consistent resource of strength for producing exclusive CFS
research findings that do not overlap psychiatric illnesses. Additionally, none
of these fields seem packed with ardent supporters of the idea that the illness
is physiological. Encephalomyelitis, they say, would make the illness
undoubtedly physiological. After all, shouldn't that be the goal of our
advocacy, rather than just landing the disease in confines of the brain?

In this case both camps are accurate about the shortcomings of the opposing
view. However, one question remains unanswered. Must the only effective
alternative to the degrading name “chronic fatigue syndrome” be wholly brain
central? And more importantly, what are the effects of a brain-central term on
us, those who the term is going to represent? Neither camp,
encephalomyelitis or
encephalopathy want to talk about this.

So much attention has been paid to what effects various suffixes would
entail, that little or no discussion has been given to the validity or the
effects of a designating the illness as brain pathology. What are
those effects? And why is it important?

The Unseen Costs of M.E.-only advocacy

Is emphasizing the brain counterproductive?

Year in and year out, researchers dealing in fields of research unrelated to
the brain have been some of the strongest supporters of the physiological basis
for CFS. Additionally, symptoms whose footprint may fall outside the brain are
also the most distinct symptoms shared by those with the disease. In the last 15
years, research on immune irregularities, circulatory abnormalities, and
metabolic dysfunction has produced some of the most exclusive findings under CFS
funding streams.

Even when the brain has been theorized to be the root cause of CFS, the
postulations have often been inconsistent and hardly exclusive to this illness.
Neuroendocrine and HPA axis research, abnormalities often cited by psychiatrists
as markers for CFS, have questionable overlaps with other fatiguing and
psychiatric illnesses, such as PTSD and anxiety disorders. Brain perfusion
abnormalities are likewise seen in many psychiatric illnesses. Isn't this
a good reason to avoid a name focusing only on brain pathology?
If not, why not?

Emphasizing brain dysfunction will not be an effective strategy in steering
away from a behavioral/psychiatric model. An increasing emphasis on brain
pathology is exactly where the behaviorists and psychiatrists are headed.
The long debated question
of whether illnesses of brain chemistry or dysfunction are behavioral or organic
is -- and will for some time continue to be -- heatedly debated.

In one such example, a leader of a clinic in the U.K. claims that encouraging
patients to view their illness as brain-central has a political and social
benefit of palliate them toward compulsory psychiatric care. He states: “The
focus on brain chemistry has the advantage- from the patient's standpoint- of
keeping their illness firmly within the bounds of soma rather than psyche. From
a social scientific point of view ... it reflects a distinctive twentieth
century understanding as to how psychiatric factors can be conceptualized…'
(Banks & Prior 2001: 19)

The preceding researcher's blend of brain pathology has questionable overlaps
with previously defined, psychiatric disorders. Unconcerned about this problem,
he continues by emphasizing brain chemistry has effectively palliated patients
to behavioral treatments for these illnesses his clinic is known for. “This was
done by introducing the concept of `brain chemistry' causations for CFS, casting
it as soma.”

Dr, Simon Wessely, a U.K researcher who often seems to relish public
limelight, holds no punches in stating where he believes the pathology of the
disease lies, "... the brain is a more likely place to look for the causes of
CFS/ME than elsewhere." He frequently bristles, in almost an insecure fashion,
at any suggestion of overstating objective microbiological or circulatory
research findings that would fall outside the brain. He adds "...psychiatric
disorders, anxiety and stress can, and do, cause changes in brain function and
chemistry, and they do. That is just a simple fact. "

Michael Sharpe is another researcher who has participated in the same school
of thought. “Modern neuroscience is reminding us that symptoms do have a
physiological basis, and these are explanations that patients find more
acceptable... Whatever their biological basis, there is strong evidence that
symptoms and disability are shaped by psychological factors.”

The scientific community must be convinced that involvement of cerebral
regions is predominant, not secondary, if a brain-central term for the illness
is to be accepted. But have we ever stopped to ask, where does this approach
lead? Are we going to emphasize HPA axis, neuroendocrine abnormalities, and
cerebral perfusion dysfunction in order to obtain the M.E. term? If we choose to
do so, the issue of whether or not these are “brain chemistry causations for
psychiatric disorders” or are influenced by behavior will remain in play.

In his book, Chronic Fatigue Syndrome: A Biological Approach, Dr. Kenny
DeMeirleir assembled a variety of talented and respected researchers from around
the globe. Taking turns, these researchers presented a compelling amount of
objective findings that established CFS as an organic and systemic illness.
These researchers did not use subjective questionnaires, neurological theories, feelings, or sociological
musings to support their ideas; rather, they used objective laboratory
instruments: Rnase L, T cell activation, and blood cell abnormalities. CFS, Demeirleir says, has microbiological roots. “Innate immunity
dysfunction would be a more accurate name for CFS.”

Neither encephalopathy nor encephalomyelitis can underscore the important
strides current research has made towards understanding CFS. Underscoring and
supporting contributions of researchers whose field of expertise lies outside
the brain is a key component to finding a cure. It is becoming increasingly
difficult to do so, and even counterproductive, with an advocacy strategy that
insists on brain pathology as primary.

Fatigue or Myalgic – Which symptom could be problematic?

It is easy to see the problems a name like “chronic fatigue” would bring.
Shortly after the name was adopted, concerned advocates warned that the term
would steer researchers down a broad and unstable path. Unfortunately, they were
right.

Chronic fatigue" is a shotgun name, and the broad term has been a detriment
to research and clinical care, as well as public awareness of CFS. If a name is
"what you make of it", "chronic fatigue" has made a potpourri. Confusion about
what CFS is, or isn’t, has been commonplace. Definitions for CFS have been
constantly broadened, and various “fatiguing” illnesses have been merged into
CFS research samples. These "fatiguing illnesses" often don’t have the hallmark
symptoms of CFS, notably severe exhaustion after exercise and circulatory
symptoms.

Symptoms chosen for a name greatly influence focus, and the symptom of
“chronic fatigue” steers just about anywhere and everywhere. One patient hits
the nail on the head when she says, “Even my friends could not understand that
I'm not 'just tired'. Almost every illness has the symptom of “chronic fatigue”.
"

M.E advocacy is perceived as a solution to this problem. But this raises an
important question: “Are there other organic myalgia-predominant illnesses being
confused with CFS? And even more succinctly, are there myalgia-predominant
illnesses in which the vast majority of patients do not have severe exercise
intolerance that is a hallmark of the disease? The answer is unequivocally,
”Yes”.

As one fibromyalgia patient states, “I would also like to change the name of
FMS (to M.E) as it doesn't fully describe the severity of its impact on
sufferers.” Another says, “CFS/ME also affects those with fibromyalgia,
Hopefully one of these days people will recognize both as legitimate
debilitating diseases.” She feels the 'myalgic' in M.E. will help recognize the
muscle pain of “Fibromyalgia, another indescribably debilitating disease that
often goes hand in hand with ME/CFS.”

When fibromyalgia funding lagged in the early 90's, a host of researchers
took the advantage the broad CFS definition afforded to fund their research.
Researchers such as Goldberg, Buchwald, and Yunus are examples of those who
claim that CFS improves with graduated exercise. These researchers tend
to emphasize myalgia, pain sensitivity, and brain pathology as the predominant
features of the illness.

Fatiguing illnesses may indeed be muddying CFS research samples. However, the
confusion created by the symptom emphasis is never a one-way street. The
term myalgia can cause confusion as much as the
term fatigue.

If the case can be made that the term “chronic fatigue” is undermining the
distinctness of the illness, then it is reasonable to suggest that emphasizing
the symptom of muscle pain (myalgia) can have the same effect. Attend a CFS support group
meeting anywhere in the U.S.. There you will find many fibromyalgia patients
whose condition improves with exercise (some very strenuous aerobic exercise)
and who show very little of the metabolic dysfunction seen in CFS. Fatiguing
illnesses are not the only illnesses that may be muddying the waters of CFS
research and diagnosis. Myalgia-predominant illnesses may perform that task as
well.

Is M.E. the only hope for a reliable Case Definition?

There is a deeper motive for taking up M.E. advocacy. The Ramsey-based
definition for M.E. emphasizes the most distinct symptom of the disease,
activity/exercise intolerance. It also highlights the distinct symptom of
circulatory dysfunction or orthostatic intolerance. These symptoms have
important clinical significance. If applied, they can lead to a more effective
diagnosis, as well as improved samples for research.

If I were to become an M.E advocate, the advantages of the M.E definition
would be my best justification. The M.E. description of Ramsey is very close to
the distinct illness that I suffer from. M.E. definition also wisely group
neurological dysfunction, rather than place each neurological symptom on equal
weight with more exclusive symptoms. However, to stop here makes two
assumptions.

First, the M.E. case definition requires patients to experience delayed
muscle recovery after exertion. Slower recovery and post-exertion symptoms are
certainly hallmark features of the illness. But in my case and the cases of many
others, post-exertional symptoms have constituted more than just slow muscle
recovery or myalgia. For many, flu-like symptoms, overwhelming metabolic
collapse are their most disabling post-exertional symptoms.

The second reason has to do not only with the need for reform, but the most
politically effective way to achieve that reform. M.E advocacy is not solely
based on advocating a definition; it is also based on advocating a term. By
demanding the case definition and the M.E. name be linked together in our
advocacy efforts, we reduce our chances of repairing either. Could it be
possible that the strength of M.E. is not the terminology of the name, but the
distinct symptoms, the simplicity, and the use of classification within the
definition? I believe it is.

Some are encouraging advocates to spend their efforts on a move to separate
CFS and M.E. Under this proposal, those with M.E would have a physiological and
distinct illness, while those with CFS would suffer from a broadly morphed
dysfunctional state. This proposal leaves behind some of the best physiological
research findings. Also, diagnosis of either CFS or M.E. would likely hinge on
the personal philosophy of individual clinicians. Even more problematic is the
fact that this proposal doesn't augment our credibility; it merely provides two
choices. Wouldn't it be better to repair the CFS definition once and for all?

We should emphasize our common goal of having distinctive, hallmark symptoms
emphasized in a new, revised case definition. However, it is politically more
feasible to gain that inclusion without inflexible insistence on the M.E term
and verbatim definition. Insisting neurological symptoms be grouped rather than
individually featured, orthostatic and circulatory symptoms be added, and the
fatigue and post-exertional symptoms of the illness be properly defined are the
most pragmatic option for successful reform.

The Great Assumption – The First Impressions Trump Card…

The most likely reason M.E. advocacy give many hope has to do with the
gravely and serious intonation of the name itself. As one M.E. advocate says,
“What's in a name? FIRST IMPRESSIONS - Everything!” Another adds, “Myalgic
encephalomyelitis sounds
serious. 'Chronic fatigue' does not.”

I vividly recall hearing a severely disabled M.E advocate describe how she
became an enthusiastic supporter of M.E advocacy. She observed the differing
reactions of her neighbors’ when she told them she had chronic fatigue syndrome
or myalgic encephalitis. Although her neighbors weren’t sure what the terms
'myalgic' or 'encephalitis' meant, they reacted much more sympathetically to
the technical reverberation than they did to the benign sounding, 'chronic
fatigue syndrome'. Based on this outcome, she felt the grave first impression 'myalgic encephalitis' conveyed was a strong justification to base her future
advocacy efforts around the term. It is undeniable, the name
myalgic
encephalitis sounds ominous. For that reason
alone, it entices many advocates as a seemingly simple approach on the road to success.

But even if M.E. was universally adopted, would this be enough to make the
controversy surrounding the illness cease? An abstruse or technically serious
name will NOT place an illness on a physiological foundation. EXCLUSIVE research
findings which are accepted by the greater scientific community, and a name that
IS BASED on that research, are!

I remember reading of a public discussion regarding the name change a few
years ago. Along with the typical support for encephalitis and encephalopathy,
there was a spattering of support expressed for terms centered on, or derived
from, neurasthenia. I found that troubling yet revealing. Neurasthenia is a term
that, like myalgic encephalitis, possesses a serious and technical resonance.
Neurasthenia was originally viewed as a physiological and disabling illness.
Today, neurasthenia is primarily considered a hysteric's disease. So, why were
patients advocating the term? Could it be that they were often allowing first
impressions to overrule long-term efforts to find a solid foundation?

Fibromyalgia is another name that has technical obscurity. Has this helped
boost Fibromyalgia awareness, funding, and treatment to levels commiserate with
the damage the illness has caused? Hardly. Technical obscurity, grave first
impressions, and serious intonation are not a trump card. An obscure term may
have short-term benefits, especially with laymen, but those short-term benefits
are not enough to replace the public or medical community's apathy with an
unshakable and lasting foundation.

The Greatest Cost of M.E. Advocacy

It is not just what M.E advocacy does that is the problem, it is what it
doesn’t do. The largest problem with M.E advocacy is that advocate's faith and
hopes are placed in something that will not -- due to real scientific and
political limitations -- deliver. This has profound and severe consequences.

I understand that some feel an advocacy style centered on the term and
tradition of M.E. has been, or is going to be, effective. However, some
advocates feel it is the ONLY way to be effective. It has no limitations. There
should be a litmus test for proposals to be “pure M.E. terminology, pure
Ramsey”. Has securing the term "encephalomyelitis" become our focus? If so, this
will be the most costly aspect of M.E advocacy.

Certainly, most advocates do not fall into that category. In fact, many would
concede that all possibilities to achieve our goals should be on the table.

But this moderation doesn't represent the entire community. Many of our most
passionate advocates are convinced that all advocacy efforts should be filtered
through the term M.E. If large portions of our
community are convinced there must be only one way to meet our objectives, then
our odds of succeeding are very limited.

Without a doubt, M.E. advocacy was born of real needs, heartfelt loss, and a
need for reform. These provide a solid base for successful advocacy. But,
successful advocacy will require flexibility, modernization, and a constant
reexamination of the our advocacy approaches. M.E advocacy can provide a good
clue to our common needs, but our methods of addressing those needs may need to
change to realize final success.

Author's note:

Hope is an important concept. Hope is indeed the engine of advocacy, change,
and progress. And admittedly, much hope has been invested in M.E. advocacy.
Perhaps it is this hope that has been one of the reasons many feel the topics
discussed here are often seen as taboo -- better left unsaid. The topics in this
op/ed have been privately discussed for years. But publicly, behind the whispers, there
has often been an intimidated silence. Get in the way of hope, and you
might find it uncomfortable.

There is hope. As a international community, we possess a common ground and
consensus that is truly remarkable, yet often ignored. This consensus transcends
borders and languages. There is widespread agreement that the term “chronic
fatigue syndrome” has made the illness a nonstarter politically and publicly.
There is also a widespread agreement that the integrative definition, which
attempts to mix various fatiguing illnesses into CFS research samples, is
unsound. And finally, there is a consensus that the physiological basis of this
illnes has long since been established. This consensus is important to remember,
as well as the common goals that we all have of finding a biomarker, increased
public awareness, and eventually, a cure.